An 83-year-old male was admitted to the Intensive Care Unit (ICU) post emergency intubation in the operating theatre for bilateral VCP of unclear origin causing airway obstruction.

Sixteen days prior to the admission to ICU, he had presented to the Emergency Department with high output (>3 litres/day) from colostomy and acute kidney injury. He was managed on the surgical ward with intravenous fluids, octreotide and loperamide. The stoma outputs remained persistently high, and he also started vomiting which required nasogastric tube insertion. Intravenous Total Parenteral Nutrition (TPN) was started to provide him with nutritional support. Gastroscopy performed on day 12 showed a normal oesophagus, bilious gastric fluid and duodenal erosions. Biopsies were taken from stomach and duodenum. Stomoscopy was normal. He was considered for reversal of colostomy.

Approximately 11 months prior to this admission he was diagnosed with locally advanced rectal adenocarcinoma located 8.5 cm from the anal verge. The rectal cancer was graded as T2N1 on pelvic MRI. There were no distant metastases on PET-CT after 4 months when he underwent loop colostomy. He was then commenced on long course chemoradiotherapy (LC-CRT) for 8 weeks with capecitabine 1500mg BD on days of radiotherapy only. Capecitabine was ceased early due to high stoma output. Six weeks prior to the current admission he underwent low anterior resection. Three weeks following the surgery he began the first cycle of CAPOX chemotherapy (Oxaliplatin 200mg on day 1 and Capecitabine 1500mg twice daily). Capecitabine was ceased at the time of his admission to hospital again due to high stoma output.

A day after commencement of chemotherapy he started complaining of difficulty in swallowing and speaking. Flexible Nasal Endoscopy (FNE) performed 4 days later at the time of admission to the hospital revealed mildly inflamed larynx suggestive of mild laryngitis and reflux, normal epiglottis, left arytenoid hooding and inability to visualise left vocal cord. Repeat FNE on the following day showed left arytenoid hooding and left vocal cord paresis with slight flickering. The right vocal cord was moving well and compensating.

He developed stridor on day 21 of his recent chemotherapy. Repeat FNE showed no supraglottic oedema, significant pooling of secretions in pyriforms and vallecula and left arytenoid hooding making it difficult to assess the vocal cord mobility. The view was repeatedly getting obstructed with secretions as the patient was unable to swallow or clear effectively with cough. Epiglottis and arytenoid had decreased sensation with no cough reflex on stimulation.

Over the next 24 hours he continued to deteriorate with ongoing stridor and desaturations. FNE was repeated and revealed bilateral vocal cord palsy in paramedian position and narrowed airway. He underwent emergency intubation in the operating theatre by anaesthetists and was admitted to ICU.

The cause of BVCP remained unclear as no local structural abnormality was found. Therefore, neurologist’s opinion was sought, and broad differential diagnoses were considered including vascular, variant of Guillain-Barre syndrome, vasculitis, infectious, inflammatory and nutritional. Magnetic Resonance Imaging (MRI) of Brain, base of skull and neck were all normal, and no central abnormalities were detected. The vasculitis screen (ANA, ENA, dsDNA, ANCA) was negative. The complement levels C3 and C4 were normal. The serum protein electrophoresis was normal, and the urine was negative for Bens Jones protein. Lupus Anticoagulant, Cardiolipin, Beta 2 Glycoprotein were not detected. The thyroid function test and serum levels of vitamin E, B6, copper and zinc were normal. The serology for hepatitis B, hepatitis C, human immunodeficiency virus and syphilis were negative. The serum angiotensin converting enzyme level was normal, thus ruling out sarcoidosis.

Various options for managing this life life-threatening condition were considered such as cordotomy, vocal cord lateralisation and surgical tracheostomy. The first two options were ruled out due to increased risk of aspiration from pooling of secretions, possibility of rebound stridor and airway distress. On day seven of intubation, the patient was taken back to the operating theatre and had a trial of extubation. Repeat FNE showed flickering of right vocal cord and immobile left vocal cord. There was only minimal glottic gap. He was reintubated and surgical tracheostomy was performed.

He was discharged to the surgical ward on day 10 of ICU admission. Subsequently he was assessed by speech pathologist and the Videofluroscopic Swallow Study (VFSS) showed small volume aspiration during swallow on thin fluids. Therefore, percutaneous endoscopic gastrotomy (PEG) tube was inserted to facilitate feeding. He was discharged home after spending four months in the hospital. He had persistent BVCP at the time of his last follow up 8 months after initial presentation.

His other past medical history included malignant neoplasm of urinary bladder (high grade invasive urothelial carcinoma, sarcomatoid variant), three years prior to the admission and was treated with intravesical BCG vaccine. Subsequent cystoscopies were normal. Three years prior to the admission, he was diagnosed with ischemic heart disease for which he underwent percutaneous intervention to left anterior descending artery.

His routine medications included amlodipine, valsartan, aspirin, atorvastatin, furosemide, calcium carbonate, Ural powder, cholecalciferol, esomeprazole, loperamide, mirtazapine, nebivolol, ondansetron, paracetamol and silver sulfadiazine topical cream.